This phenomenon has been explained that HAX1‐riched EVs promote angiogenesis through the activation of the FAK pathway in endothelial cells by increasing the expression levels of ITGB6 (Figure 5B).[106] In chronic myeloid leukemia (CML) xenograft models, mice treated with EVs from CML cells had larger tumors than controls treated with PBS.[107] Anti‐apoptotic molecules like BCL‐w, BCL‐xl and survivin have been found to increase while pro‐apoptotic molecules like BAD, BAX, and PUMA have been found reduced both in vitro and in vivo samples. The gene discussed is ITGB6; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.